IM14.1-14 | Obesity — Practice Quiz

Correct. Asian-Indian BMI thresholds are: overweight ≥23 kg/m² and obese ≥25 kg/m². This patient's BMI of 24.9 falls in the overweight range (≥23 but <25). Using Western thresholds (overweight ≥25) would have missed this classification entirely. Additionally, his waist circumference of 93 cm exceeds the Asian-Indian cut-off for men (≥90 cm), confirming abdominal obesity.

Asian-Indian BMI cut-offs: overweight ≥23 kg/m², obese ≥25 kg/m². Waist circumference cut-offs: men ≥90 cm, women ≥80 cm. These lower thresholds reflect greater visceral fat accumulation at lower BMI in South Asians.

Asian-Indian BMI cut-offs are lower than Western thresholds: overweight ≥23 kg/m², obese ≥25 kg/m². A BMI of 24.9 in an Indian patient is in the overweight category. This lower threshold reflects the greater accumulation of visceral fat at lower BMI values in South Asians compared to Europeans.

Correct. The clinical features — fatigue, constipation, dry skin, periorbital puffiness, cold intolerance, and gradual weight gain — form the classic symptom cluster of hypothyroidism. TSH is the most sensitive single test for primary hypothyroidism and should be the first investigation when this secondary cause is suspected. Hypothyroidism is the most common secondary cause of obesity in clinical practice.

Secondary causes of obesity: hypothyroidism (most common — screen with TSH), Cushing syndrome (low-dose dexamethasone suppression test), hypothalamic disease, polycystic ovary syndrome (PCOS in women), and drug-induced obesity (steroids, antipsychotics, insulin, antiepileptics). Match the clinical pattern to the investigation.

The symptom cluster here (fatigue, constipation, dry skin, periorbital puffiness, cold intolerance) strongly suggests hypothyroidism — the most common secondary cause of obesity. TSH is the most sensitive screening test. Cushing syndrome would present with centripetal fat distribution, striae, hypertension, and glucose intolerance; cortisol testing would be appropriate for that pattern.

Correct. Prader-Willi syndrome (PWS) is caused by loss of paternal imprinting at 15q11-q13. Clinical features include: hypotonia and feeding difficulty in infancy, followed by hyperphagia and obesity from early childhood, intellectual disability, hypogonadism, almond-shaped eyes, small hands and feet, and short stature. The familial occurrence in brothers (with paternal transmission) is consistent with PWS.

Syndromic obesity clues: Prader-Willi (hyperphagia + intellectual disability + hypogonadism + small hands/almond eyes); Bardet-Biedl (retinal dystrophy + polydactyly + renal anomalies); Alstrom (retinal dystrophy + deafness + dilated cardiomyopathy). MC4R mutation = most common monogenic obesity without syndromic features.

The constellation of childhood-onset severe obesity, intellectual disability, hypogonadism, almond-shaped eyes, small hands, and short stature is classic for Prader-Willi syndrome (chromosome 15q11-q13 imprinting defect). Bardet-Biedl syndrome presents with retinal dystrophy (progressive visual loss), polydactyly, and renal anomalies. MC4R mutation is the most common monogenic cause of obesity but causes severe hyperphagia without the additional syndromic features.

Correct. IDF 2005 criteria require central obesity as mandatory (waist ≥90 cm in Asian men — met: 92 cm) PLUS any 2 of: triglycerides ≥150 mg/dL (met: 190), HDL <40 mg/dL in men (met: 35), BP ≥130/85 mmHg (met: 134/86), fasting glucose ≥100 mg/dL (met: 112). He meets ALL 4 remaining criteria, so metabolic syndrome is confirmed. Pre-diabetic fasting glucose (100–125 mg/dL) counts for this criterion — diabetes diagnosis is not required.

IDF metabolic syndrome (Asian): central obesity mandatory (waist ≥90 cm men, ≥80 cm women) + ≥2 of: TG ≥150, HDL <40/<50 (M/F), BP ≥130/85, FBG ≥100. NCEP-ATP III requires any 3 of 5 (no single mandatory criterion). State which criteria set you are using — the question will specify or you should document both.

IDF metabolic syndrome criteria: mandatory central obesity (waist ≥90 cm in Asian men) PLUS ≥2 of: TG ≥150 mg/dL, HDL <40 mg/dL (men), BP ≥130/85 mmHg, fasting glucose ≥100 mg/dL. This patient meets central obesity (92 cm) and all 4 remaining criteria. A fasting glucose of 112 mg/dL (pre-diabetic, not diabetic) still meets the metabolic syndrome glucose criterion.

Correct. This case illustrates the classic obesogenic environment: (1) ultra-processed food availability at the worksite, (2) shift-work-driven circadian disruption which dysregulates ghrelin/leptin rhythms and increases appetite for high-calorie food, (3) short sleep duration independently predicts weight gain, and (4) a built environment without active-transport or exercise infrastructure. These environmental determinants drive the obesity epidemic beyond what genetic variation alone can explain.

Environmental determinants of obesity: shift work + sleep deprivation (ghrelin/leptin dysregulation), ultra-processed food environment, built environment discouraging physical activity, screen time, stress-driven eating. The gene pool has not changed in 30 years — the environment has.

The driving factors here are all environmental: shift-work circadian disruption (elevates ghrelin, suppresses leptin, promotes high-calorie food intake), short sleep (<7 hours is independently associated with obesity), food environment (ultra-processed snack availability), and built environment (no parks, long commute). These are environmental determinants of obesity — the primary explanation for the global epidemic that cannot be attributed to genetics alone.

Correct. Olanzapine (and other second-generation antipsychotics such as clozapine and quetiapine) causes weight gain primarily through histamine H1 and serotonin 5-HT2C receptor antagonism, which increases appetite and promotes carbohydrate craving. Olanzapine is among the antipsychotics with the greatest propensity for metabolic side effects, including weight gain (average +4.2 kg at 10 weeks), glucose dysregulation, and dyslipidaemia.

Drug-induced obesity: antipsychotics (olanzapine > clozapine > quetiapine — via H1/5-HT2C), glucocorticoids (Cushingoid fat distribution), insulin/sulfonylureas, antiepileptics (valproate, carbamazepine), tricyclics. Always take a complete medication history in obesity evaluation.

Olanzapine causes weight gain through H1 (antihistamine) and 5-HT2C (antiserotonin) receptor antagonism — both pathways increase appetite and carbohydrate craving. It is one of the highest-risk antipsychotics for metabolic side effects. Drug-induced obesity (steroids, antipsychotics, insulin, antiepileptics, antidepressants) is an important secondary cause to identify in the obesity history.

Correct. The clinical triad of centripetal obesity (buffalo hump, moon facies), violaceous striae (stretch marks with a purple-red hue indicating thin, collagen-poor skin from hypercortisolism), hypertension, glucose intolerance, and hypokalaemia is the classic presentation of Cushing syndrome. The overnight 1 mg dexamethasone suppression test is the first-line screening test — a morning cortisol <50 nmol/L (1.8 µg/dL) excludes Cushing syndrome in most cases.

Cushing syndrome screening: overnight 1 mg DST (first-line), 24-hour urine free cortisol, or late-night salivary cortisol. Distinguish simple obesity (white striae, BP usually lower, no moon facies) from Cushing syndrome (violaceous striae, centripetal distribution, hypertension, glucose intolerance, hypokalaemia).

Buffalo hump, moon facies, violaceous (not white) striae, hypertension, glucose intolerance, and hypokalaemia together strongly suggest Cushing syndrome. The overnight 1 mg dexamethasone suppression test is the recommended first-line screening test. A serum TSH would be appropriate if the clinical picture suggested hypothyroidism (dry skin, cold intolerance, constipation) — not this florid Cushingoid picture.

Correct. Non-judgmental counselling requires: (1) acknowledging the patient's feelings and effort before delivering advice, (2) reframing non-adherence as a biological challenge — the brain is wired for high-calorie food in an obesogenic environment, not a moral failure, (3) using motivational interviewing to explore barriers rather than repeating directives. The 5As framework (Ask, Assess, Advise, Agree, Assist) structures this approach. Immediate pharmacotherapy is not indicated when the issue is the quality of lifestyle counselling support.

Non-judgmental obesity counselling: use person-first language ('person with obesity' not 'obese person'), acknowledge effort, reframe non-adherence biologically (hormonal, environmental — not willpower failure), use motivational interviewing (open questions, reflective listening, 5As framework). Premature pharmacotherapy without addressing counselling quality is inappropriate.

The correct response to a patient expressing weight-loss failure as self-blame is to use person-first, non-judgmental language: acknowledge effort, validate difficulty, reframe as biological not moral. Non-adherence to lifestyle modification is the expected outcome of a brain designed for a food-scarce environment now encountering an obesogenic one — it is not a character failure. Explore barriers using motivational interviewing before escalating to pharmacotherapy.

Correct. Semaglutide (a GLP-1 receptor agonist) is indicated for weight management and achieves 10–15% weight reduction in clinical trials (STEP programme) with superior efficacy to orlistat or phentermine. In patients with type 2 diabetes, GLP-1 RAs provide concurrent glycaemic improvement and, for semaglutide specifically, proven cardiovascular outcome benefit (SELECT trial: 20% reduction in MACE in non-diabetic obese patients). Indication in India: pharmacotherapy is indicated when BMI ≥27.5 with comorbidities (diabetes qualifies) and lifestyle modification has failed to achieve ≥5% weight loss over 3–6 months.

Obesity pharmacotherapy indications (Indian guidelines): BMI ≥27.5 with comorbidities or ≥32.5 kg/m² alone, after ≥3–6 months lifestyle failure. Preferred agents: GLP-1 RAs (semaglutide/liraglutide) — best efficacy + CV benefit. Orlistat: modest efficacy, GI side effects (steatorrhoea). Phentermine/topiramate: not licensed in India. Avoid if cardiac disease, uncontrolled hypertension, pregnancy.

GLP-1 receptor agonists (semaglutide, liraglutide) are the preferred pharmacotherapy for obesity with type 2 diabetes — they reduce weight (10–15%), improve glycaemia, and semaglutide has proven cardiovascular outcome benefit (SELECT trial). Orlistat causes GI side effects and achieves only 2.9 kg additional weight loss vs placebo. Phentermine is a short-term sympathomimetic contraindicated in hypertension, cardiovascular disease. The indication for pharmacotherapy is BMI ≥27.5 with comorbidities or ≥32.5 without comorbidities.

Correct. The Obesity Surgery Society of India (OSSI) and IFSO-APC guidelines for Asian Indians use lowered BMI thresholds: bariatric surgery is indicated at BMI ≥32.5 kg/m² with at least one major comorbidity (type 2 diabetes, obstructive sleep apnoea, hypertension, dyslipidaemia, NASH) or BMI ≥37.5 kg/m² without comorbidities. These are lower than the Western thresholds (≥35 with comorbidities, ≥40 without) in recognition of the greater metabolic risk at lower BMI in Asian Indians.

Asian-Indian bariatric surgery thresholds (OSSI): BMI ≥32.5 with comorbidity, or ≥37.5 without comorbidity. Western thresholds (≥35/≥40) are not applicable. Comorbidities qualifying: T2DM, OSA, HTN, dyslipidaemia, NASH. Procedures: sleeve gastrectomy (commonest in India), Roux-en-Y gastric bypass (best diabetes remission), adjustable gastric band (falling out of use).

Asian-Indian bariatric thresholds are lower than Western standards: ≥32.5 kg/m² with comorbidity or ≥37.5 without (vs Western ≥35/≥40). This patient with BMI 42, diabetes, sleep apnoea, and hypertension clearly qualifies. The most metabolically beneficial procedure for T2DM is Roux-en-Y gastric bypass (highest diabetes remission rates) or sleeve gastrectomy. Bariatric surgery achieves 50–70% excess weight loss at 5 years — far superior to lifestyle or pharmacotherapy alone.